Acute cardiovascular response to high altitude in healthy and anemic subjects: a mathematical model

The acute cardiovascular response to hypocapnic hypoxia (simulating high altitude condition) is investigated both in healthy and anemic subjects by using a mathematical model of short-term cardiovascular regulation. The model includes a description of the cardiovascular system and several control mechanisms triggered by changes in blood gas content. Hypoxia produces significant rise in cardiac output and heart rate, while arterial pressure remains almost unchanged. Coronary blood flow augments enormously, maintaining constant oxygen delivery to the heart. However, heart oxygen consumption rises dramatically, to sustain the increased power of the cardiac pump during hypoxia. Cerebral blood flow increases to a less extent, because of the vasconstrictor influence of hypocapnia on cerebral vessels; its increase is not sufficient to maintain oxygen delivery in the brain. Model suggests that a critical level for aerobic metabolism in the heart and brain is reached at an arterial oxygen pressure (PaO₂) of about 25 mmHg. Anemia during normoxia is compensated by an increase in cardiac output, local vasodilation, and an increase in oxygen extraction. Since the regulatory mechanisms are already recruited in basal conditions, the compensatory reserve exhausts prematurely during hypocapnic hypoxia. A critical level for vital functions is already reached at PaO₂ of 45 mmHg.